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In this model, gene duplication events are facilitated by Alu sequences, so called junction Alus, that duplicated adjacent sequences regardless of their relative orientation and position to that sequence [25].
One major shortcoming of our simulation study is that it does not explicitly model gene duplication.
Our simulation system does not explicitly model gene duplication, and worse, we do not know the true alignment of repeats in the ancestral genomic material, so it is impossible to quantify the accuracy of glocal aligners using our evaluation scheme.
In this model, gene duplication is followed by divergence and HD; in the divergence process links are removed from duplicated nodes with a uniform probability α, and in the HD process a new link is established between two duplicated nodes with another probability β, forming a heterodimer [29], [30].
For the TDRL model, gene duplication is necessary, which can be achieved by replication slippage in single stranded templates.
Much as how restrictive pleiotropy can decouple two phenotypes in our model, gene duplication allows the two gene copies to evolve freely.
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Instead, we indirectly model gene duplications in two ways.
It is also possible to generalise this framework by explicitly modeling gene duplications, adding the possibility of multiplicities as in Wittler and Stoye (2010).
To model changes in gene copy number, we simply changed the corresponding probability of transcription, for example, to model a gene duplication event, we multiplied the probability of that gene's transcription by two.
First, to generate a template PPI network with the characteristics of real yeast PPI networks, we used a geometric graph model with gene duplication and mutation (GEO-GD expansion model; Przulj et al., 2010; Supplementary Fig. S3A).
Here we quantify this effect by using genomic content as a model for gene duplication by specifically focusing on X-linked genes, such that these genes are "duplicated" in female individuals (XX) relative to male individuals (XY).
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